Resistance of novel mouse strains different in MHC class I and the NKC domain to the development of experimental tumors

  • Authors:
    • Anna Fišerová
    • Jan Richter
    • Katarína Čapková
    • Jana Bieblová
    • Romana Mikyšková
    • Milan Reiniš
    • Marie Indrová
  • View Affiliations

  • Published online on: June 3, 2016     https://doi.org/10.3892/ijo.2016.3561
  • Pages: 763-772
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Abstract

To elucidate the immunological mechanisms critical for tumor progression, we bred novel mouse strains, different in the NKC and H-2D domains. We used inbreeding to generate hybrids of Balb/c and C57BL/6 of stable H-2Db+d-NK1.1neg and H-2Db-d+NK1.1high phenotypes. We analyzed the growth of three established MHC class I-deficient tumor cell lines: TC-1/A9 tumor (HPV-associated) and B16F10 melanoma, both syngeneic to C57BL/6, and the MCB8 (3-methycholanthrene-induced tumor) syngeneic to Balb/c. Furthermore, we induced colorectal carcinoma by azoxymethane-DSS treatment to test the susceptibility to chemically-induced primary cancer. We found that the novel strains spontaneously regressed the tumor transplants syngeneic to both Balb/c (MCB8) and C57BL/6 (B16F10 and TC-1/A9) mice. The H2-Db+d-NK1.1neg, but not the H2-Db-d+NK1.1high strain was also highly resistant to chemically-induced colorectal cancer in comparison to the parental mice. The immune changes during TC-1/A9 cancer development involved an increase of the NK cell distribution in the peripheral blood and spleen along with higher expression of NKG2D activation antigen; this was in correlation with the time-dependent rise of cytotoxic activity in comparison to C57BL/6 mice. The TC-1/A9 cancer regression was accompanied by higher proportion of B cells in the spleen and B220+/CD86+ activated antigen-presenting B cells distributed in the lymphoid organs, as well as in the periphery. The changes in the T-cell population were represented mainly by the prevalence of T helper cells reflected by grown CD4/CD8 ratio, most prominent in the b+d-NK1.1neg strain. The results of the present study imply usefulness of the two novel mouse strains as an experimental model for further studies of tumor resistance mechanisms.
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August-2016
Volume 49 Issue 2

Print ISSN: 1019-6439
Online ISSN:1791-2423

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Spandidos Publications style
Fišerová A, Richter J, Čapková K, Bieblová J, Mikyšková R, Reiniš M and Indrová M: Resistance of novel mouse strains different in MHC class I and the NKC domain to the development of experimental tumors. Int J Oncol 49: 763-772, 2016
APA
Fišerová, A., Richter, J., Čapková, K., Bieblová, J., Mikyšková, R., Reiniš, M., & Indrová, M. (2016). Resistance of novel mouse strains different in MHC class I and the NKC domain to the development of experimental tumors. International Journal of Oncology, 49, 763-772. https://doi.org/10.3892/ijo.2016.3561
MLA
Fišerová, A., Richter, J., Čapková, K., Bieblová, J., Mikyšková, R., Reiniš, M., Indrová, M."Resistance of novel mouse strains different in MHC class I and the NKC domain to the development of experimental tumors". International Journal of Oncology 49.2 (2016): 763-772.
Chicago
Fišerová, A., Richter, J., Čapková, K., Bieblová, J., Mikyšková, R., Reiniš, M., Indrová, M."Resistance of novel mouse strains different in MHC class I and the NKC domain to the development of experimental tumors". International Journal of Oncology 49, no. 2 (2016): 763-772. https://doi.org/10.3892/ijo.2016.3561